Could extracellular vesicles derived from mesenchymal stem cells be a potential therapy for acute pancreatitis-induced cardiac injury?

Acute pancreatitis (AP) often leads to a high incidence of cardiac injury, posing significant challenges in the treatment of severe AP and contributing to increased mortality rates. Mesenchymal stem cells (MSCs) release bioactive molecules that participate in various inflammatory diseases. Similarly, extracellular vesicles (EVs) secreted by MSCs have garnered extensive attention due to their comparable anti-inflammatory effects to MSCs and their potential to avoid risks associated with cell transplantation. Recently, the therapeutic potential of MSCs-EVs in various inflammatory diseases, including sepsis and AP, has gained increasing recognition. Although preclinical research on the utilization of MSCs-EVs in AP-induced cardiac injury is limited, several studies have demonstrated the positive effects of MSCs-EVs in regulating inflammation and immunity in sepsis-induced cardiac injury and cardiovascular diseases. Furthermore, clinical studies have been conducted on the therapeutic application of MSCs-EVs for some other diseases, wherein the contents of these EVs could be deliberately modified through prior modulation of MSCs. Consequently, we hypothesize that MSCs-EVs hold promise as a potential therapy for AP-induced cardiac injury. This paper aims to discuss this topic. However, additional research is essential to comprehensively elucidate the underlying mechanisms of MSCs-EVs in treating AP-induced cardiac injury, as well as to ascertain their safety and efficacy.

Tanshinone IIA improves sepsis-induced acute lung injury through the ROCK2/NF-κB axis.

BACKGROUND: This research sought to explore the effects of Tanshinone IIA (TIIA) and its potential mechanism in sepsis-induced acute lung injury. METHODS: Cecal ligation and puncture (CLP) was performed to construct a sepsis model in vivo. RLE-6TN cells were treated with lipopolysaccharide (LPS) to establish a sepsis model for in vitro experiments. The histopathological changes of the lung tissues were scored using HE staining, IHC, and dry and wet method. Apoptosis in the lung tissues was detected by TUNEL assay. Meanwhile, ELISA was used to determine the levels of the pro-inflammatory factors. Cell proliferation and apoptosis were evaluated using CCK-8, EdU assays and flow cytometry, respectively. RT-qPCR analysis was carried out to measure the expression of Rho associated coiled-coil containing protein kinase 2 (ROCK2). RESULTS: TIIA dramatically alleviated the pathological injuries of the lung, and relieved apoptosis, neutrophil infiltration, lung edema and inflammation response. Highly expressed ROCK2 was observed in septic rats in vivo and LPS-induced RLE-6TN cells in vitro. We found that ROCK2 knockdown promoted cell proliferation, and inhibited cell apoptosis and inflammation in LPS-treated RLE-6TN cells. Moreover, TIIA improved LPS-caused injury in RLE-6TN cells through downregulating ROCK2 expression. Mechanistically, TIIA repressed LPS-caused activation of the NF-κB pathway by regulating ROCK2 in RLE-6TN cells. Additionally, TIIA assuaged CLP-induced lung injury in the rats via downregulating ROCK2 to inactivate the NF-κB pathway in vivo. CONCLUSION: Our data demonstrated that TIIA improved sepsis-induced lung injury by downregulating ROCK2 and further inactivating the NF-κB signaling pathway in vivo and in vitro.

Accumulated Clinical Experiences from Successful Treatment of 1377 Severe and Critically Ill COVID-19 Cases.

In late December 2019, COVID-19 was firstly recognized in Wuhan, China and spread rapidly to all of the provinces of China. The West Campus of Wuhan Union Hospital, the designated hospital to admit and treat the severe and critically ill COVID-19 cases, has treated a large number of such patients with great success and obtained lots of valuable experiences based on the Chinese guideline (V7.0). To standardize and share the treatment procedures of severe and critically ill cases, Wuhan Union Hospital has established a working group and formulated an operational recommendation, including the monitoring, early warning indicators, and several treatment principles for severe and critically ill cases. The treatment experiences may provide some constructive suggestions for treating the severe and critically ill COVID-19 cases all over the world.

Development a clinical prediction model of the neurological outcome for patients with coma and survived 24 hours after cardiopulmonary resuscitation.

BACKGROUND: Cardiac arrest is still a global public health problem at present. The neurological outcome is the core indicator of the prognosis of cardiac arrest. However, there is no effective means or tools to predict the neurological outcome of patients with coma and survived 24 hours after successful cardiopulmonary resuscitation (CPR). HYPOTHESIS: Therefore, we expect to construct a prediction model to predict the neurological outcome for patients with coma and survived 24 hours after successful CPR. METHODS: A retrospective cohort study was used to construct a prediction model of the neurological function for patients with coma and survived 24 hours after successful CPR. From January 2007 to December 2015, a total of 262 patients met the inclusion and exclusion criteria. RESULTS: The predictive model was developed using preselected variables by a systematic review of the literature. Finally, we get five sets of models (three sets of construction models and two sets of internal verification models) which with similar predictive value. The stepwise model, which including seven variables (age, noncardiac etiology, nonshockable rhythm, bystander CPR, total epinephrine dose, APTT, and SOFA score), was the simplest model, so we choose it as our final predictive model. The area under the ROC curve (AUC), specificity, and sensitivity of the stepwise model were respectively 0.82 (0.77, 0.87), 0.72and 0.82. The AUC, specificity, and sensitivity of the bootstrap stepwise (BS stepwise) model were respectively 0.82 (0.77, 0.87), 0.71, and 0.82. CONCLUSION: This new and validated predictive model may provide individualized estimates of neurological function for patients with coma and survived 24 hours after successful CPR using readily obtained clinical risk factors. External validation studies are required further to demonstrate the model's accuracy in diverse patient populations.

Higher body mass index is not a protective risk factor for 28-days mortality in critically ill patients with acute kidney injury undergoing continuous renal replacement therapy.

Background: Acute kidney injury (AKI) requiring continuous renal replacement therapy (CRRT) is a fatal and common clinical disorder in critically ill patients. Recent studies have shown that the relationship between BMI and the outcome of patients with AKI undergoing CRRT is conflicting. Methods: A retrospective cohort study based on data reuse. Univariate analysis, multi-factor regression analysis and subgroup analyses were used to explore the association of the BMI with the 28-days mortality risk in patients with AKI undergoing CRRT. Results: From January 2009 to September 2016, a total of 1120 cases met the inclusion criteria and were enrolled in this study. The univariate analysis showed that BMI was associated with 28-days mortality of patients with AKI undergoing CRRT, its HR value was 0.98 (0.96, 0.99). The multi-factor regression analysis showed that BMI was not associated with 28-days mortality of patients with AKI undergoing CRRT in the four models, the adjusted HR value of four models were 1.00 (0.96, 1.04), 1.01 (0.97, 1.04), 1.00 (0.96, 1.04) and 1.00 (0.96, 1.04), respectively. The subgroups analyses showed that the BMI was a risk factor of the 28-days mortality in patients with AKI undergoing CRRT when GFR ≥30 mL/min, its HR value was 1.04 (1.01, 1.09). Conclusion: Higher BMI was not a protective risk of 28-day mortality in patients with AKI undergoing CRRT. Especially, when GFR ≥30 mL/min, higher BMI increased the risk of the 28-day mortality rate in patients with AKI undergoing CRRT.

The related factors for the recovery and maintenance time of sinus rhythm in hospitalized patients with cardiopulmonary resuscitation: A single-center retrospective case-control study.

No matter in or outside hospital, the success rate of cardiopulmonary resuscitation (CPR) is very low. The sign of successful CPR is the recovery of spontaneous circulation. The premise of the recovery of spontaneous circulation is the recovery and maintenance of sinus rhythm, but there is still no related research.We aim to study the factors for the recovery and maintenance time of sinus rhythm in patients with CPR.A single-center retrospective case-control study.Ethical review was obtained (ethical approval number: 20180031).The second affiliated hospital of Xi'an Jiaotong University, Xi'an Shaanxi, China.From January 2011 to December 2016, totally 344 cases met the inclusion and exclusion criteria, sinus rhythm recovered group (SR group) (n = 130 cases), sinus rhythm unrecovered group (SUR group) (n = 214 cases).The multivariate logistic regression analysis showed that red blood cell counts (OR = 1.30, 95% CI:1.04-1.63, P = .02), rescue time (OR = 0.95, 95% CI:0.94-0.97, P <.001), the usage of norepinephrine (OR = 2.14, 95% CI:1.06-4.35, P = .04) were important factor for the recovery of sinus rhythm in patients with CPR. Multivariate linear regression analysis showed that the dosage of epinephrine, the usage of naloxone and diagnosis were important factors for maintenance time of sinus rhythm after resuscitation, P <.05. The rescue time had high accuracy to predict the recovery of sinus rhythm, the area under the receiver operator characteristic (ROC) curve (AUC) was 0.84 (0.80, 0.88), sensitivity and specificity are respectively 71.54% and 93.46%.Red blood cell counts, the rescue time and the usage of norepinephrine might be important factors for the recovery of sinus rhythm, and the dosage of epinephrine, the usage of naloxone and the diagnosis might be important factors for the maintenance time of sinus rhythm in patients with CPR.

Zoledronic acid sensitizes rhabdomyosarcoma cells to cytolysis mediated by human γδ T cells.

Rhabdomyosarcoma (RMS) is the most common type of soft-tissue sarcoma in children. Immunotherapy has been proposed as a treatment for this deadly tumor. In the present study, the cytotoxicity of ex vivo expanded γδ T cells on RMS cell lines was evaluated and the molecular interactions involved were investigated. γδ T cells were expanded in vitro using peripheral blood mononuclear cells from 5 healthy donors and were stimulated with zoledronic acid (Zol) and interleukin 2. RMS cell lines RD and A-673 were used as target cells. The cytotoxicity of the γδ T cells against RMS was assessed in vitro and in vivo. γδ T cells were cytotoxic to RMS cells. Importantly, Zol markedly increased their cytotoxic potential. RMS cells treated with Zol-stimulated γδ T cells to produce interferon γ. γδ T cell-mediated cytotoxicity was primarily through the T cell receptor-dependent signaling pathway in blocking studies. Transfer of γδ T cells together with Zol into nude mice induced the regression of RD tumor xenotransplants. The results of the present study provide the rationale for the clinical evaluation of γδ T cells in RMS.

Pregnancy complicated with agranulocytosis.

RATIONALE: Pregnancy is a complicated physiological process. Physiological leukocytosis often takes place and it is primarily related to the increased circulation of neutrophils, especially during the last trimester of pregnancy. Noncongenital agranulocytosis during pregnancy is rare and reported only occasionally, while in most of the cases, the agranulocytosis has already occurred prior to pregnancy or induced by identified factors such as antibiotics, antithyroid agents, or cytotoxic agents. Gestation-induced agranulocytosis has not been reported, so we present a case of gestation-induced agranulocytosis in this article. PATIENTS CONCERN: In this case, we present a Chinese woman (aged 25) in her 38th week of the first gestation who had the complication of agranulocytosis. No abnormality was detected in regular examinations before pregnancy and in the first trimester. Since the last trimester of pregnancy, the patient began to suffer from agranulocytosis and intermittent fever, the maximum being temperature 38.8°C. At admission, the neutrophil granulocytes were 0.17 × 10 L and the bone marrow biopsy showed that agranulocytosis was detected, but the levels of red blood cell and megalokaryocyte were normal. In addition, antinuclear antibodies were detected at a dilution of 1:40, but anti-dsDNA, antiphospholipid antibody, and neutrophil granulocyte antibody were negative. DIAGNOSES: The patient was empirically treated as having pneumonia. INTERVENTIONS: We tried to use granulocyte colony-stimulating factor, γ-globulin, glucocorticoids, antibiotics, and antifungi agents to treat the patient, but her symptoms were not alleviated until the patient had a cesarean section. OUTCOMES: After 24 hours of cesarean section, the temperature and neutrophil granulocyte returned to normal. After a year of follow-up, we found that the patient and the baby were healthy. LESSONS: Agranulocytosis during pregnancy seems to be associated with immunosuppression induced by immunoregulations and termination of pregnancy may be effective for refractory pregnancy complicated with agranulocytosis, but further studies are needed to confirm this.

Preoxygenation using invasive ventilator in volume control mode in patients with emergency intubation can shorten the time of preoxygenation and improve the quality of preoxygenation: A retrospective study.

Preoxygenation can rapidly improve oxygenation and enhance the security of endotracheal intubation, so it is very essential before endotracheal intubation. The conventional preoxygenation method self-inflating bag (SIB) is not very effective in case of emergency. So our study aims to find a more effective method of preoxygenation in a critical situation.We retrospectively analyzed data of 105 patients in this study. A total of 49 patients with preoxygenation with invasive ventilator in volume control mode (VCM) and 56 patients with preoxygenation with SIB were included. No significant differences were detected in the baseline data of the 2 groups (P > 0.05). Time of preoxygenation (95%) was 174 (168-180) seconds in group VCM and 205 (199-212) seconds in group SIB (P < 0.05), and multifactor linear regression showed that its main risk factors were the methods of preoxygenation and PO2 before preoxygenation (P < 0.05). Immediate SPO2 after preoxygenation was 91 (89-92)% in group VCM and 85 (83-86)% in group SIB (P < 0.05). Total time of preoxygenation and intubation was 266 (252-280) seconds in group VCM and 318 (298-338) seconds in group SIB (P < 0.05). The 24-hour and overall survival rate in group SIB were lower than in group VCM (P > 0.05). Cox regression showed that SaO2 at 5 minutes after intubation was the major risk factor for the survival rate.Invasive ventilator with volume control mode can shorten the time of preoxygenation and improve the quality of preoxygenation in patients with emergency intubation and may be a better method of preoxygenation in a critical situation.

ß-elemene enhances the radiosensitivity of gastric cancer cells by inhibiting Pak1 activation.

AIM: To explore the potential of ß-elemene as a radiosensitizer for gastric cancer cells and the underlying mechanisms. METHODS: SGC7901, MKN45, MKN28, N87, and AGS human gastric cancer cell lines were used to screen for radioresistant gastric cancer cell lines. A 3-(4,5-dimeth-ylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assay was used to determine the effects of ß-elemene and IPA-3 on cell viability in MKN45 and SGC7901 gastric cancer cell lines. A clonogenic survival assay and annexin V-FITC/PI apoptosis detection assay were used to evaluate cellular radiosensitivity and radiation-induced cell death, respectively. A proteomic method, isobaric tags for relative and absolute quantitation (iTRAQ), was employed to screen the proteins regulated by ß-elemene pretreatment prior to ionizing radiation (IR) in SGC7901 gastric cancer cell line. IPA-3 was used as a specific small molecule inhibitor of p21-activated protein kinase 1 (Pak1) to target Pak1 signaling. Protein levels of PAK1IP1 (p21-activated protein kinase-interacting protein 1), total Pak1 (t-Pak1), phospho-Pak1 (T423), phospho-ERK1/2 (Thr202/Tyr204), and cleaved caspase-3 (17 kDa) were assessed by western blotting. RESULTS: MKN45 and SGC7901 gastric cancer cell lines were relatively more resistant to IR. ß-elemene pretreatment decreased clonogenic survival following IR in MKN45 and SGC7901 gastric cancer cell lines. Additionally, ß-elemene pretreatment prior to IR increased radiation-induced cell death compared with IR alone in MKN45 (10.4% ± 0.9% vs 34.8% ± 2.8%, P < 0.05) and SGC7901 (11.6% ± 0.9% vs 46.7% ± 5.2%, P < 0.05) human gastric cancer cell lines, respectively, consistent with the level of cleaved caspase-3 (17 kDa). Through iTRAQ analysis and western blot validation, we found that ß-elemene upregulated PAK1IP1 and downregulated phospho-Pak1 (T423) and phospho-ERK1/2 in SGC7901 gastric cancer cells. IR increased the level of phospho-Pak1 (T423). Pretreatment with ß-elemene decreased radiation-induced Pak1 and ERK1/2 phosphorylation. Inhibition of Pak1 using IPA-3 decreased clonogenic survival following IR. In addition, IPA-3 increased radiation-induced cell death in MKN45 (13.4% ± 0.3% vs 26.6% ± 1.0%, P < 0.05) and SGC7901 (16.0% ± 0.6% vs 37.3% ± 1.7%, P < 0.05) gastric cancer cell lines, respectively, consistent with the level of cleaved caspase-3 (17 kDa). Western blotting showed that IPA-3 decreased radiation-induced Pak1 and ERK1/2 phosphorylation. CONCLUSION: This is the first demonstration that ß-elemene enhances radiosensitivity of gastric cancer cells, and that the mechanism involves inhibition of Pak1 signaling.

miR-186 and 326 predict the prognosis of pancreatic ductal adenocarcinoma and affect the proliferation and migration of cancer cells.

MicroRNAs can function as key tumor suppressors or oncogenes and act as biomarkers for cancer diagnosis or prognosis. Although high-throughput assays have revealed many miRNA biomarkers for pancreatic ductal adenocarcinoma (PDAC), only a few have been validated in independent populations or investigated for functional significance in PDAC pathogenesis. In this study, we correlated the expression of 36 potentially prognostic miRNAs within PDAC tissue with clinico-pathological features and survival in 151 Chinese patients. We then analyzed the functional roles and target genes of two miRNAs in PDAC development. We found that high expression of miR-186 and miR-326 predict poor and improved survival, respectively. miR-186 was over-expressed in PDAC patients compared with controls, especially in patients with large tumors (>2 cm), lymph node metastasis, or short-term survival (< 24 months). In contrast, miR-326 was down-regulated in patients compared with controls and displayed relatively increased expression in the patients with long-term survival or without venous invasion. Functional experiments revealed that PDAC cell proliferation and migration was decreased following inhibition and enhanced following over-expression of miR-186. In contrast, it was enhanced following inhibition and decreased after over-expression of miR-326. A luciferase assay indicated that miR-186 can bind directly to the 3'-UTR of NR5A2 to repress gene expression. These findings suggest that miR-186 over-expression contributes to the invasive potential of PDAC, likely via suppression of NR5A2, thereby leading to a poor prognosis; high miR-326 expression prolongs survival likely via the decreasing invasive potential of PDAC cells. These two miRNAs can be used as markers for clinical diagnosis and prognosis, and they represent therapeutic targets for PDAC.

Anticancer effects of ß-elemene in gastric cancer cells and its potential underlying proteins: a proteomic study.

Gastric cancer is a common malignancy with a poor prognosis. ß-elemene is a broad-spectrum anticancer drug extracted from the traditional Chinese medicinal herb Curcuma wenyujin. In the present study, we investigated the anticancer effects of ß-elemene in gastric cancer cells and the potential proteins involved. Human SGC7901 and MKN45 gastric cancer cells were treated with different concentrations of ß-elemene. Cell viability, clonogenic survival and apoptotic cell death were assessed. ß-elemene inhibited viability and decreased clonogenic survival of gastric cancer cells in a dose-dependent manner. Apoptosis induction contributed to the anticancer effects. We then employed a proteomic method, isobaric tags for relative and absolute quantitation (iTRAQ), to detect the proteins altered by ß-elemene. In total, 147 upregulated proteins and 86 downregulated proteins were identified in response to ß-elemene treatment in SGC7901 gastric cancer cells. Among them, expression of p21-activated protein kinase­interacting protein 1 (PAK1IP1), Bcl-2-associated transcription factor 1 (BTF) and topoisomerase 2-α (TOPIIα) were validated by western blot analyses and the trends were consistent with iTRAQ results. Top pathways involved in ß-elemene treatment in SGC7901 gastric cancer cells included ribosome signaling, peroxisome proliferator-activated receptors (PPARs) signaling pathway, regulation of actin cytoskeleton, phagosome, biosynthesis and metabolism of some amino acids. Collectively, our results suggest a promising therapeutic role of ß-elemene in gastric cancer. The differentially expressed proteins provide further insight into the potential mechanisms involved in gastric cancer treatment using ß-elemene.

Diet-induced obesity promotes murine gastric cancer growth through a nampt/sirt1/c-myc positive feedback loop.

Obesity increases the risk of gastric cancer and may promote its growth, as was recently demonstrated by our novel in vivo mouse model. However, the underlying mechanisms of this correlation remain unclear. The purpose of this study was to investigate the precise effects of obesity on gastric cancer growth and to elucidate the potential molecular mechanisms. Diet-induced obese mice were insulin-resistant, glucose-intolerant and had high serum visfatin concentration. In the subcutaneous mouse model, tumors were more aggressive in diet-induced obese mice compared with lean mice. Tumor weights showed a significant positive correlation with mouse body weights, as well as serum insulin and visfatin concentrations. Immunohistochemical staining showed that the expression levels of iNampt, Sirt1 and c-MYC proteins were upregulated in the subcutaneous tumors from obese mice compared to those from lean animals. Furthermore, obesity not only prompted significantly murine forestomach carcinoma cell migration, proliferation, but also affected cellular apoptosis and cell cycle by endocrine mechanisms. These were associated with increased expression of the pro-survival nampt/sirt1/c-myc positive feedback loop confirmed by RT-PCR and western blotting. These results suggested that diet-induced obesity could promote murine gastric cancer growth by upregulating the expression of the nampt, sirt1 and c-myc genes.

Diet-induced obesity potentiates the growth of gastric cancer in mice.

Obesity increases the risk of gastric cancer and may affect its development and progression, however, the mechanisms underlying this association are completely unknown. The purpose of the current study was to investigate the effect of obesity on gastric cancer growth by adopting a novel in vivo model. Diet-induced obese and lean mice were inoculated with murine forestomach carcinoma cells, and studied for 2 weeks. Tumor histology, cellular proliferation and apoptosis were evaluated. Serum glucose, insulin, visfatin levels and peripheral CD3(+), CD4(+/-), CD8(+/-) lymphocytes were assayed. All mice were alive and developed no metastasis, a greater number of obese mice developed palpable tumors than lean mice. The tumors from obese mice had a larger volume, greater intratumoral adipocyte mass, and exhibited a higher proliferation and reduced apoptosis rate compared to those of lean animals. Both serum insulin and visfatin concentrations correlated positively with tumor proliferation and negatively with tumor apoptosis. Obese mice had a significantly lower level of CD3(+), CD3(+)CD4(+) T lymphocytes, and a lower level of CD4(+)/CD8(+) in peripheral blood compared to these lymphocyte levels in the lean mice. In conclusion, the altered adipocytokine milieu and insulin resistance observed in obesity may lead directly to alterations in the tumor microenvironment and cell immunity for avoiding cancer, thereby, promoting gastric cancer survival and growth.

Relation among p130Cas, E-cadherin and beta-catenin expression, clinicopathologic significance and prognosis in human hepatocellular carcinoma.

BACKGROUND: p130Cas (p130Crk-associated substance) is a junction protein that is important to the adhesion between cytoskeleton and extracellular matrix. Also, the adhesion molecules E-cadherin and beta-catenin play important roles in the invasiveness of carcinoma. This study was undertaken to investigate the effects of p130Cas, E-cadherin and beta-catenin on the invasion, metastasis and prognosis of hepatocellular carcinoma (HCC). METHODS: Immunohistochemistry was used to evaluate the expression of p130Cas, E-cadherin, and beta-catenin in 40 patients with HCC. All patients were followed up postoperatively, and the relationship between expression and clinicopathological prognostic parameters was analyzed. RESULTS: The positive expression rates of p130Cas and E-cadherin in HCC tissue (n=40) were 62.50% and 55.00%, but in normal liver tissue 10%, and 100%, respectively (P<0.05). The abnormal expression rate of beta-catenin in HCC tissue was 70%, while in normal liver tissue it was 13.33% (P<0.05). The positive rate of p130Cas was correlated with lymph node invasion, pathological stage, TNM stage, and a worse prognosis, but not with gender, age, HBV infection, hepatic cirrhosis, alpha-fetoprotein (AFP) level before operation, and tumor diameter. Similarly, the expression of E-cadherin and beta-catenin was correlated with lymph node invasion, pathological stage, TNM stage, and worse prognosis, but not with gender, age, HBV infection, hepatic cirrhosis, AFP level before operation, and tumor size. Correlations were found between p130Cas and abnormal E-cadherin/beta-catenin expression (P<0.001 and <0.05, respectively). CONCLUSIONS: In HCC, there is a negative correlation between the positive expression of p130Cas and the normal expression of the adhesion molecules E-cadherin/beta-catenin, and p130Cas plays important roles in the invasion, metastasis and prognosis of HCC. p130Cas may be involved in alterating the structure and function of E-cadherin/beta-catenin, by regulating tyrosine phosphorylation via the p130Cas-Src signal pathway.

[Plasma levels of ascorbic acid and vitamin E in patients with liver cirrhosis].

OBJECTIVE: To investigate the plasma levels of ascorbic acid and vitamin E in patients with liver cirrhosis and to explore their significance. METHODS: The plasma levels of ascorbic acid,vitamin E and lipoperoxides in patients with liver cirrhosis were measured, and the results were compared with those of sex-and age-matched healthy subjects. RESULT: The plasma levels of ascorbic acid, vitamin E and lipoperoxides in the patients group were (42.94 +/-6.99)micromol/L, (17.99 +/-3.51)micromol/L and (14.09 +/-1.28)micromol/L, respectively, while those in the control group were (53.30 +/-9.45)micromol/L (t=9.50, P=0.000), (24.59 +/-7.22)micromol/L (t=7.94, P=0.000) and (12.11 +/-1.20)micromol/L (t=17.21, P=0.000), respectively. CONCLUSION: The levels of ascorbic acid and vitamin E in patients with liver cirrhosis decrease significantly,which may indicates the disturbance of balance between oxidation and antioxidation.